Pre‐exposure to Subtoxic Levels Prevents Kainic Acid Lesions in Organotypic Hippocampal Slice Cultures: Effects of Kainic Acid on Parvalbumin‐immunoreactive Neurons and Expression of Heat Shock Protein 72 Following the Induction of Tolerance

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Abstract
The effects of kainic acid on the survival of principal neurons and parvalbumin‐immunoreactive (PARV‐IR) neurons, and on the expression of heat shock protein 72 immunoreactivity (HSP72‐IR) were investigated in organotypic hippocampal slice cultures. Untreated cultures displayed an organotypic organization and the development and morphology of PARV‐IR neurons in the hippocampus paralleled that reported to occur in vivo, with the exception of the hilar region of the dentate gyrus which exhibited a marked lack of PARV‐IR neurons. No constitutive expression of HSP72 was found in untreated cultures. The lesion of CA3 neurons and the reduction in numbers of PARV‐IR neurons in both CA3 and CA1 after chronic exposure to 5 μM kainic acid were similar to those reported to occur in vivo. Exposure to 1 μM doses of kainic acid resulted in a widespread appearance of HSP72‐IR and the induction of tolerance to a previously toxic dose of kainic acid. These results suggest the presence of endogenous neuroprotective mechanisms, activated by a stress response which induces HSP72, and is reminiscent of the induced tolerance reported to occur after a mild ischaemic insult.